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Related Experiment Video

Updated: Jun 4, 2026

Exogenous Administration of Microsomes-associated Alpha-synuclein Aggregates to Primary Neurons As a Powerful Cell Model of Fibrils Formation

Exogenous Administration of Microsomes-associated Alpha-synuclein Aggregates to Primary Neurons As a Powerful Cell Model of Fibrils Formation

Published on: June 26, 2018

Lysosomal dysfunction increases exosome-mediated alpha-synuclein release and transmission.

Lydia Alvarez-Erviti¹, Yiqi Seow, Anthony H Schapira

¹University Department of Clinical Neurosciences, Institute of Neurology, University College London, UK. l.alvarez@medsch.ucl.ac.uk

Neurobiology of Disease

|February 10, 2011

Summary

Exosomes facilitate the spread of alpha-synuclein, a key protein in Parkinson's disease (PD). Lysosomal dysfunction in PD accelerates this exosome-mediated transmission, highlighting a potential therapeutic target.

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Exogenous Administration of Microsomes-associated Alpha-synuclein Aggregates to Primary Neurons As a Powerful Cell Model of Fibrils Formation

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Published on: June 26, 2018

Generation of Alpha-Synuclein Preformed Fibrils from Monomers and Use In Vivo

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Evaluation of LC3-II Release via Extracellular Vesicles in Relation to the Accumulation of Intracellular LC3-positive Vesicles

Evaluation of LC3-II Release via Extracellular Vesicles in Relation to the Accumulation of Intracellular LC3-positive Vesicles

Published on: October 18, 2024

Area of Science:

Neuroscience
Cell Biology
Pathology

Background:

Alpha-synuclein aggregation is central to Parkinson's disease (PD) pathology.
Cell-to-cell transmission of alpha-synuclein may drive PD's anatomical spread.

Purpose of the Study:

To investigate the role of exosomes in alpha-synuclein release and transmission.
To determine if lysosomal dysfunction, relevant to PD, affects this process.

Main Methods:

Exosomes were isolated from alpha-synuclein over-expressing cells.
Alpha-synuclein content in exosomes and its transfer to recipient cells were analyzed.
Cells were treated with ammonium chloride or bafilomycin A1 to induce lysosomal dysfunction.

Main Results:

Exosomes released from alpha-synuclein over-expressing cells contained alpha-synuclein.
These exosomes efficiently transferred alpha-synuclein to normal cells.
Lysosomal dysfunction increased exosome-mediated alpha-synuclein release and transmission.

Conclusions:

Exosomes are crucial for both the release and intercellular transmission of alpha-synuclein.
Parkinson's disease-associated factors, like lysosomal dysfunction, enhance this transmission.
Targeting exosome-mediated alpha-synuclein spread represents a potential therapeutic strategy for Parkinson's disease.